The underlying etiology of the patient's problems was heatstroke. This condition is defined as the combination of hyperthermia (core temperature >105°F [40.6°C]) and neurologic impairment.[1] Two types of heatstroke are recognized: classic nonexertional heatstroke (NEHS) and exertional heatstroke (EHS).[1] From 1979 to 1997, the National Centers for Health Statistics (NCHS) reported 7,046 deaths secondary to heat, or 371 deaths per year; this is presumed to underestimate the true numbers of deaths. Those older than age 65 years make up almost half of these cases.[1] Heatstroke is seen less often in subtropical areas than in temperate climates. The 2003 heat wave in France is attributed for the deaths of more than 10,000 people.[2]
The 80% mortality rate associated with heatstroke can be reduced to as low as 10% if heatstroke is recognized early and cooling treatment is initiated promptly. The damage caused by this condition is directly related to the temperature and the length of time it remains elevated. The classic presentation is that of hyperthermia, anhidrosis, and neurologic deficit. Some patients, however, still sweat, and others begin to cool en route to the hospital; these patients might not meet the classic temperature criteria.[1]
Classic NEHS occurs most frequently in very young and very old individuals during heat waves. Individuals with alcoholism are also at risk for NEHS, the chronically or mentally ill, and those who are dehydrated. Patients present with high temperatures, lack of sweating, and altered mental status. Neurologic complaints may include irritability, lethargy, confusion, ataxia, seizures, and coma. Psychiatric-type symptoms, such as delusions or hallucinations, can also occur. The classic triad is not always present. Sweating may occur, and patients may present with temperatures <105.8°F (41°C).[1] Additional symptoms and signs may include vomiting, diarrhea, tachycardia, hypotension, and tachypnea.
EHS typically occurs in healthy young patients participating in vigorous physical activity in hot environments,[1] but it can occur at ambient temperatures as low as 70°F (21.1°C) as well.[3] Those affected with EHS present with hyperthermia, altered mental status, and diaphoresis. They can exhibit strange behaviors or syncope during physical activity, as well as experience abdominal cramps, nausea, vomiting, diarrhea, headache, and dizziness. Because these patients retain their ability to sweat, their temperatures may drop after physical activity has stopped but before presentation at the ED. Risk factors for EHS include viral infections, fatigue, dehydration, the use of stimulants, and not being acclimatized to higher temperatures.
In addition to elevated temperatures and neurologic signs and symptoms, other organ systems may also be affected in EHS, including the cardiovascular, pulmonary, gastrointestinal, hepatic, renal, and musculoskeletal systems.[1] The stress caused to the cardiovascular system can be particularly worrisome in the elderly. Tachycardia at 130-140 beats/min and greater is common, as is hypotension resulting from dehydration, redistribution of blood to the skin, and collapse of vascular tone. Patients can be tachypneic and hypoxic for various reasons, including atelectasis, noncardiogenic pulmonary edema, and aspiration.[1] Liver and renal failure can pose serious risks to those surviving the neurologic insult.[3] Rhabdomyolysis is common and, along with hypotension, often leads to renal failure. Liver failure also commonly occurs, possibly secondary to direct heat injury and hypoxia.[2,3,4,5] Disseminated intravascular coagulation may also occur.[5]
Multisystem damage is a result of the widespread deadly cellular effects of heat and the body's resultant inflammatory response. Multisystem injury leads to increased morbidity and mortality. In a retrospective study on heatstroke victims, Varghese et al found that the overall mortality rate was 70% for all cases, but it was 85% in patients with multiorgan failure. These investigators found that elevation of creatine kinase, elevation of liver transaminases, and metabolic acidosis were each predictors of poor patient prognosis.[2]
The differential diagnosis of heatstroke includes entities in many categories, including thyroid storm, pheochromocytoma, sepsis, meningitis/encephalitis, alcohol withdrawal, and abuse of stimulants (among others). Anticholinergic and antipsychotic drugs rarely cause fever, except in rare cases of neuroleptic malignant syndrome, but these agents can place a patient at risk for heatstroke by preventing sweating. Such drugs include antihistamines, antiparkinsonian drugs, neuroleptics, and others.[6] Another life-threatening condition secondary to exposure to certain drugs is malignant hyperthermia (MH). This condition can lead to an uncontrolled rise in body temperature in susceptible individuals from exposure to volatile anesthetics during general anesthesia, nearly all gas anesthetics, and the neuromuscular blocking agent succinylcholine. The clinician must keep a high level of suspicion for heatstroke because, in some cases, it may present insidiously and valuable time may be lost to investigating other possible diagnoses (as shown in a study by Varghese et al, in which patients presented a mean of 4.1 days after the onset of elevated temperature).[2]
Given the possibility of multisystem failure, many diagnostic tests are appropriate for suspected heatstroke; these include complete blood cell (CBC) count, chemistries, liver function tests, creatine kinase, troponin, urinalysis and urine culture, blood cultures, chest radiography, and ECG. A CT scan of the brain may identify alternative causes of altered mental status.[1] A toxicology screen may, in some cases, be useful as well.
Hypokalemia can occur early on in heatstroke; however, hyperkalemia can possibly occur secondary to muscle damage. Moreover, rhabdomyolysis can lead to creatine kinase levels greater than 100,000 U/L. A urinalysis showing marked hematuria on urine dipstick interpretation but few red blood cells (RBCs) on microscopic analysis is consistent with myoglobin in the urine and rhabdomyolysis. Blood urea nitrogen (BUN) and creatinine measurements may detect renal failure, which may result from dehydration, heat injury to the kidney, and rhabdomyolysis (or even all three). Liver transaminases can be elevated into the thousands or even tens of thousands as a result of liver and/or muscle injury. A rise in troponin level is not uncommon in NEHS, particularly in the elderly; in fact, it was associated, among other parameters, with a higher level of mortality in a study of victims of the 2003 French heat wave.[7] The etiology of elevated troponin in this setting remains unclear.[8]
Among illicit drugs, cocaine has been associated with a higher incidence of death secondary to hyperthermia. Marzuk et al concluded that, of patients younger than 55 years dying from hyperthermia in New York City, one-fourth had taken cocaine immediately beforehand. Moreover, these investigators showed that there were one third more deaths secondary to cocaine use on days hotter than 88°F (31.1°C). They concluded that cocaine is singular among drugs in its association with hyperthermia and mortality.[9] A small study of 8 patients presenting with heatstroke during the 1998 New Orleans heat wave found cocaine was associated more often with heat-related illness than were other drugs and medications.[6]
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Cite this: Andréa B. Lese, Rick G. Kulkarni. Altered Mental Status in a Young Man Picked Up On the Street - Medscape - Aug 24, 2010.
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